MPN
Myeloproliferative neoplasms (MPNs) are rare cancers and include diseases of the blood and bone marrow. MPNs involve dysregulation at the multipotent hematopoietic stem cell (CD34). MPNs occur when the bone marrow produces too many red blood cells, platelets, or certain white blood cells. The primary subtypes include myelofibrosis, polycythemia vera, and essential thrombocythemia.
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Raajit Rampal, MD, PhD, and the "Blood Cancer Talks" hosts discuss the diagnosis and management of essential thrombocythemia.
The primary endpoint was overall best response after blast-reduction therapy.
Momelotinib and ruxolitinib improved bone marrow fibrosis, but changes were not associated with improved outcomes in MF.
Dr. Harrison discusses her current clinical research, building community with MPN Voice, and her journey into hematology.
A drug approval specific to CMML would catalyze a surge of interest in the hematology-oncology community.
Nicolaus Kröger, MD, discusses a study on GVHD and its impact on relapse in patients with myelofibrosis undergoing HSCT.
Myelofibrosis, a rare blood cancer, affects four to six per 100,000 individuals in the United States.
An international working group collaborating with the EBMT and ELN updated the 2015 guidelines for HSCT in myelofibrosis.
Ruxolitinib plus pelabresib was well tolerated and improved spleen and symptom burden in patients with myelofibrosis.
Parsaclisib plus ruxolitinib can improve symptoms and spleen volume in certain patients with myelofibrosis.
Sanjay Patel, MD, discusses a study on spatial mapping of human hematopoiesis using bone marrow tissue.
FREEDOM2 is a phase III study comparing fedratinib with best available therapy as a second-line treatment for myelofibrosis.
“Among the high-risk splicing mutations, SRSF2 has the worst prognostic role,” Dr. Braish and colleagues wrote.
The REVEAL study identified five risk factors, including leukocytosis, duration of time with PV, and more.
The treatment led to reduced hepcidin levels when used alone or in combination with ruxolitinib.
Venugopal highlights myelofibrosis research at ASH 2023.
Real-world databases lent insight into how often patients with PV experience thromboembolic events.
Dr. Al-Ali covers data on combined BET and JAK inhibition for patients with myelofibrosis presented at the 2023 ASH Meeting.
Worse survival in single-hit TP53 patients was mainly driven by bone marrow fibrosis.
SRSF2 and SF3B1 were the most common splicing mutations, followed by U2AF1 and ZRSR2.
Knowing who is at high risk in the near term could make it easier to conduct trials of anti-thrombotic therapies.
Developed by Protagonist Therapeutics, rusfertide is a novel injectable synthetic mimetic of the natural hormone hepcidin.
CALR and MPL mutations, which are associated with better outcomes, showed earlier mutation clearance than JAK2.
The retrospective study used data on 105 million U.S. patients with linked medical and prescription claims from 2007 to 2019.
Mass spectrometry–based proteomics were used to learn more about how MKs drive bone marrow fibrosis.
Prevalence of symptoms was assessed with the Myeloproliferative Neoplasm Symptom Assessment Form Total Symptom Score.
The retrospective study evaluated if pacritinib increased PLT counts in the phase III PERSIST-2 and phase II PAC203 studies.
Tasquinimod inhibited interaction of A9, a protein associated with poor prognosis.
DT2216 alone was effective, but exhibited a slightly greater cell viability reduction when combined with other therapies.
Responses in hemoglobin, white blood cell, and platelet were 75%, 82%, and 74%, respectively, at 24 weeks.
Multivariable modeling showed a notable reduction in the risk of GVHD or relapse in the ATG group.
Hemoglobin and platelets are correlated with OS, while mutations in ASXL1, EZH2, IDH1/2, U2AF1, and SRSF2 are not.
Rusfertide quickly induced hematocrit control and maintained improved levels over time in patients with polycythemia vera.
Subjectivity of morphological assessment and overlapping pathological features of subtypes can hamper accurate MPN diagnosis.
Bomedemstat is an oral lysine-specific demethylase-1 (LSD1) inhibitor clinically active in patients with MPNs.
The model could be helpful in understanding fibrotic progression in JAK2V617F mutation–positive MPNs.
The study aimed to address “a substantial unmet need for therapies that alter disease trajectory" in patients with MF.
Ruben Mesa, MD, discussed the results at the 65th ASH Annual Meeting and Exposition.
Researchers analyzed PV patients allocated to the ropeginterferon alfa-2b arm of the PROUD-PV/CONTINUATION-PV studies.
The use of combination therapies including XPO1 inhibitor selinexor is a potentially effective therapeutic strategy in MF.
This is just one finding from a longitudinal analysis of phase III data from the SIMPLIFY-1 and MOMENTUM trials.
Review more from the post-hoc time-dependent analysis of the phase III Simplify-1, Simplify-2, and MOMENTUM trials.
Led by Dr. Lindsay Rein, the goal of the phase I/II trial was to evaluate the safety and efficacy of TP-3654.
The multicenter trial studied genetic mutations across three cohorts.
CR rates were comparable in both treatment groups, but OS was superior in the ruxolitinib group.
Researchers also observed potential disease modification via rapid stabilization of platelets and stable hemoglobin levels.
There were no significant differences in response rates with pegylated interferon-alpha versus hydroxyurea in MPN treatment.
The trial is based on “compelling data” from arm III of the ongoing phase II MANIFEST study.
Primary myelofibrosis developed secondary neoplasms earlier and at higher rates versus other myeloproliferative neoplasms.
Essential thrombocythemia with CALR mutations had a higher risk of progression to myelofibrosis compared with JAK2 mutations.
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